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16 Cards in this Set
- Front
- Back
toxicities of all TNF alpha inhibitors used in treatment of RA...
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infection, lymphoma, hepatotoxicity, hematological effects HS reactions, CVS toxicity...
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tnf alpha inhibs and biological agents give to RA patient when...
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other DMARDs as mono therapy have failed
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given by IV infusion in combination with oral methotrexate at 0, 2, 6 weeks, and then once every 8
HS infusion reaction may occur - can give acetaminophen or diphenhydramine (h1block) Use for RA, together with methotrex -also for ankylosing spondylitis or crohn's hman/mouse chimeric IgG1 monoclonal ab, against TNF alpha. binds both bound and soluble tnf-a higher affinity than other biological drugs that are soluble receptors |
inflixamab
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MOA
binds to soluble and membrane bound TNF alpha SC injection every 14 days. self administered injection pen. use for RA, ankylosing spondylitis, crown's MOA -blocks TNFa reduces levels of C reactive protein reduces ESR reduces serum IL 6 reduces matrix metallo proteinases MMP 1 and 3 (secreted by fibroblast in response to cytokines. degrade the matrix) half life of 2 weeks is increased in patines also taking methotrexate BLACK BOX TB invasive funal infections opportunistics AEs exacerbates chronic CHF serious infections Lupus like syndrome its a fully humanized monoclonal IgG1 antibody |
adalimumab
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a soluble tnf a RECEPTOR
binds soluble and membrane bound tnf a use for moderate to severe RA AEs injection site reaction autoantibody formation HS reactions infections increased risk of cancer Contrain: documented HS sepsis concurrent live vaccinations SC injection once a week |
etanercept
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recombinant for of human IL-1 receptor antagonist
extracted from e. coli short half life give daily. binds to IL 1 receptor and decreases production of inflammatory cytokines use for RA AEs headache gastro injection site reaction is strong Serious AEs infections** decrease white cell antibody formation against the drug itself |
anakinra
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these DMARDS are...
-slow to act (months) no direct analgesic actions slow course of disease given to NSAID non responders and non compliant its, and those with serious GIT problems with NSAIDS and steroids -to patients whose joints are deteriorating rapidly -for juvenile RA |
D-penicillamine
chloroquine and hydroxy- sulfonamide plus salicylate=sulfasalazine |
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symptoms alleviated: reductes # of T lymphs, IL 1, RF, and inhibits macros
MOA UNKNOWN. use if other drugs have failed in RA patients major use is Wilson's disease (it chelates copper) take orally, plasma concentrations peak 1-2 hrs, but doesn't become clinically effective for months ***platelets, CBC and urinalysis before and therapy and then every 2-4 weeks. see AEs AEs cutaneous lesions blood dyscrasias - BM SUPPRESSION proteinuiria (when RA pts develop this, switch out of DMARD class altogether, don't substitute new DMARD) HS reactions (highly contrained in goodpastures syndrome) -M.Gravis can be induced by long term use teratogenic |
penicillamine
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second line RA drugs
MOA suppresses responsiveness of T lymphs to mitogens -decreassed leukocyte chemotaxid -stabalizes lysosomal membranes (where the drug concentrates) -inhibits DNA and RNA synth -traps free radicals, reducing oxidative reactions which may be ass'd with deteriorating bone take after meals. 4-12 weeks before discernible improvements seen AEs are mild -dermatitis myopathy reversible corneal opacity GI irritation nightmares *irreversible retinal degernation - dose and freq. related. opthalmic exam every six months. symptoms: night blindness, blurred vision, missing or blanched out areas of central or peripheral fields, light flashes/streaks/photophobia |
hydroxychloroquine
chloroquine |
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prodrug used for ulcerative colitis, RA, IBD, and RA
oral, then metabolized by gut bacteria to 5-aminosalicylic acid aka mesalamine aka sulfapyridine. inhibition of cyclooxygenases in the gut, diminished PG production slow acetylators have increased incidence of AEs NVD, anorrexia, rash and serum sickness. *leukopenia, thrombocytopenia, allopecia, elevated liver enzymes: occur within first 3-6 months then abate. reverse when treatment stops. |
sulfasalazine
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most commonly prescribed DMARD
used in combo with anti-TNF reduces signs and symptoms and slows progression AEs NVD leucopenia lung issues... HS reaction (can develop anytime during use) hepatotoxicity (slow, with accumulative dosing. long term -> hepatic fibrosis) |
methotrexate
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use for moderate to severe RA and psoriatic arthritis
inhitbits pyrimidine synthesis inhibits T and B roliferations |
leflunomide
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inhibits the reabsorption of urate FROM TEH LUMEN at the PT.
oral bound to albumin 90% -free drug passes into the glomerular filtrate, but more is actively secreted into the PT, where it may diffuse back because of its high lipid solubility (if given in sub tx doses, actually inhibit the secretion of the compound they are meant to increase excretion of) |
probenicid
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the 'other' uricosuric
inhibits reabsorption in PT |
sulphinpyrazone
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for long term tx of gout. not acute.
prevents production of uric acid metabolized by key enzyme, and its metabolite inhibits that enzyme, competitively, reducing production of uric acid INTERACTIONS 1 - drug increases the half life of probenicid... and probenicid increases the clearance of the drug's active metabolite. thus increase dose of allopurinol 2 - active metabolite decreases metabolism of azathiaprine and mercaptopurine. decrease doses of both. 3 - if given with theophylline (a xanthine), leads to an increased accumulation of 1-methyl xanthine, the active metabolite of theophylline (?) |
allopurinol
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unique antiinflammatory, effective only against acute gouty arthritis
reduces pain and swelling <12 hrs MOA inhibits cells division: binds to tubulin, preventing microtubules inhibits leukocyte migration into joints blocks lipoxygenase enzymes, thus blocking in inflammatory leukotrienes dramatic pain relief oral/IV interhepatic reciurculation drug secretion into bile mediated by MDR protein pump drugs that inhibit MDR... lower dose of "" side effects limit chronic usage: serious GI toxicity myelosuppressive agranulocytosis aplastic anemia myopathy alopecia |
colchicine
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